Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China (mainland).
Institute of Urology, Anhui Medical University, Hefei, Anhui, China (mainland).
Med Sci Monit. 2019 Nov 12;25:8534-8543. doi: 10.12659/MSM.917333.
BACKGROUND Eriocalyxin B (EriB), a diterpenoid isolated from the plant Isodon eriocalyx, has been shown to possess anti-tumor properties. However, few systematic studies of the mechanism underlying the anti-tumor activity of Eriocalyxin B in prostate cancer cells have been published. The aim of this study was to investigate the effect of Eriocalyxin B on prostate cancer cells. MATERIAL AND METHODS In the present study, the PC-3 (androgen-independent) and 22RV1 (androgen-dependent) human prostate cancer cell lines were cultured with and without increasing doses of Eriocalyxin B. MTT assay was used to measure cell viability. Western blotting was performed to measure levels of proteins associated with apoptosis and autophagy. Flow cytometry was used to assess changes in cell apoptosis and cycle. Fluorescence microscopy was used to capture images of autophagy-related proteins. RESULTS Treatment of human prostate cancer cells with Eriocalyxin B resulted in apoptosis in a dose- and time-dependent manner. Eriocalyxin B also induced autophagy, with elevated LC3B-II protein expression and punctuate patterns. Additionally, autophagy protected prostate cancer cells from apoptosis induced by Eriocalyxin B, which was demonstrated by addition of chloroquine (CQ). Moreover, the results indicated that Eriocalyxin B could inhibit the phosphorylation of Akt and mTOR. Eriocalyxin B induced apoptosis and autophagy by inhibition of the Akt/mTOR pathway. CONCLUSIONS Eriocalyxin B induces apoptosis and autophagy involving the Akt/mTOR pathway in prostate cancer cells in vitro. These findings provide evidence for Eriocalyxin B as a potent therapeutic for the treatment of prostate cancer.
从植物黄芩中分离得到的二萜类化合物埃里卡醇 B(EriB)已被证明具有抗肿瘤特性。然而,关于埃里卡醇 B 抑制前列腺癌细胞活性的机制的系统研究较少。本研究旨在探讨埃里卡醇 B 对前列腺癌细胞的影响。
在本研究中,培养了人前列腺癌细胞株 PC-3(雄激素非依赖性)和 22RV1(雄激素依赖性),并分别用和不用递增剂量的埃里卡醇 B 处理。MTT 法检测细胞活力。Western blot 检测与细胞凋亡和自噬相关的蛋白水平。流式细胞术检测细胞凋亡和周期变化。荧光显微镜观察自噬相关蛋白的变化。
埃里卡醇 B 处理人前列腺癌细胞可导致细胞凋亡,且呈剂量和时间依赖性。埃里卡醇 B 还诱导自噬,LC3B-II 蛋白表达增加,出现点状模式。此外,自噬可保护前列腺癌细胞免受埃里卡醇 B 诱导的凋亡,这一作用可被氯喹(CQ)阻断。此外,结果表明埃里卡醇 B 可抑制 Akt 和 mTOR 的磷酸化。埃里卡醇 B 通过抑制 Akt/mTOR 通路诱导细胞凋亡和自噬。
埃里卡醇 B 通过抑制 Akt/mTOR 通路诱导前列腺癌细胞发生凋亡和自噬。这些发现为埃里卡醇 B 作为治疗前列腺癌的有效药物提供了证据。